Subarachnoid Hemorrhage and Vasospasm as its Complication: A Review

Background: Subarachnoid hemorrhage (SAH) is an impairment in mechanical intracranial vascular system. Traumatic factor such as head trauma may lead to SAH due to rupture of leptomeningeal vessels. The most common finding in non-traumatic SAH is aneurysm rupture or arteriovenous malformation. Vasospasm is one of the most complication found in SAH, along with rebleeding and hydrocephalus. It is a delayed and self-limited condition. Despite all of that, cerebral vasospasm related with worse outcome. Although numerous study has been conducted, the exact mechanism of this phenomenon remain poorly understood. Objective: This review underlines the pathophysiological review of cerebral vasospasm as complication of SAH in order to elucidate its mechanism and improve its treatment. Conclusion: cerebral vasospasm frequently found in SAH patients. Its mechanism remains a complex one. Hemoglobin degradation may lead to bilirubin-oxidized fragments (BOXes), which responsible for constriction of the arteries. Oxidative stress and free radical’s formation contribute to the occurrence of vasospasm via PKC signaling pathway, Rho-kinase, and other molecules. Endothelin 1 (ET-1) and nitric oxide (NO) also have significant role in its mechanism. Membrane function impairment may lead to increase of calcium influx, resulting in constriction of blood vessels.